Breathlessness and Control of Breathing (awake)

Question 1

Is tidal expiration an active or passive process?

Answer 1

Passive - due to the natural recoil of the lungs

Question 2

State the equation for minute ventilation.

Answer 2

VE = VT x Frequency 
Frequency = 60/TTOT (if you want it per minute)

Question 3

How can this equation be manipulated to include TI?

Answer 3

VE = VT/TI x TI/TTOT

Question 4

What does VT/TI represent?

Answer 4

Neural Drive - mean inspiratory flow

Question 5

What does TI/TTOT represent?

Answer 5

Inspiratory Duty Cycle

Proportion of the cycle spent actively ventilating (i.e. breathing in)

Question 6

How do these factors change when there is an increase in metabolic demand?

Answer 6

Increased metabolic demand —> increased ventilation
VT/TI = INCREASE
TTOT = DECREASE (increase frequency)
TTOT is decreased by a combination of reduction in TI and TE

Question 7

What is the normal tidal volume and normal minute ventilation?

Answer 7

Tidal Volume = 0.5 L
Minute Ventilation = 6 L/min
Breathing Rate = 12 breaths per minute

Question 8

What changes take place if you use a noseclip?

Answer 8

Breathe more DEEPLY - increase in VT
Breathe SLOWER - decrease in frequency
Ventilation remains the SAME

Question 9

What changes take place when artificial dead space is added?

Answer 9

Compared to with mouthpiece only:
Minute ventilation = INCREASE
VT = INCREASE
Frequency = INCREASE 
VT/TI = INCREASE

Question 10

How is the breathing of someone with COPD different to a normal person?

Answer 10

Breathing is SHALLOWER and FASTER

Question 11

What changes when we exercise?

Answer 11

Increases neural drive and hence ventilation 
Increases frequency (decrease TTOT)

Question 12

Where is the voluntary and involuntary control of breathing located?

Answer 12

Voluntary = Cerebral Cortex 
Involuntary = Medulla

Question 13

How is the metabolic controller reset in sleep?

Answer 13

PCO2 rises

Question 14

Where, in the motor homunculus, is behavioural control of breathing located?

Answer 14

Between the hip and the trunk

Question 15

Which receptors are involved in regulating the involuntary control of breathing?

Answer 15

HYDROGEN ION RECEPTORS found in the carotid bodies and in the metabolic centre itself

Question 16

Where are the peripheral chemoreceptors located?

Answer 16

Carotid bodies (at the junction of the internal and external carotids)

Question 17

Where are the pacemakers for respiratory breathing located?

Answer 17

Medulla

Question 18

What is the main group of neurons that are involved in generating respiratory rhythm?

Answer 18

Pre-Botzinger Complex

Question 19

What muscles are affected by respiratory augmenting?

Answer 19

Pharynx, larynx and airways = inspiratory augmenting

Expiratory muscles = expiratory augmenting

Question 20

Describe the Hering-breuer reflex. Which nerve is involved?

Answer 20

Vagus Nerve (cranial nerve X)
Pulmonary stretch receptors are activated by large airway/lung inflation leading to a CUT OFF signal for inspiration  
IMPORTANT: changes in proton concentration mirrors changes in PCO2.

Question 21

Describe the carbon dioxide challenge and what it shows.

Answer 21

Changes in arterial PCO2 are induced by asking a subject to breathe in and out of a bag with a fixed volume of oxygen and primed with 7% CO2.
Re-breathing means that arterial PCO2 rises at a constant rate
The rise in PCO2 is accompanied by a pronounced rise in minute ventilation

Question 22

How does hypoxia affect the acute CO2 response?

Answer 22

Hypoxia increases the sensitivity of the acute CO2 response.

With hypoxia, there is an even GREATER rise in minute ventilation per 1 kPa rise in PCO2.

Question 23

How does chronic metabolic acidosis affect the PCO2 threshold that gives a minimal drive to breathe?

Answer 23

Chronic metabolic acidosis shifts the line to the left - a lower PCO2 is needed to cause an increase in minute ventilation
Chronic metabolic alkalosis does the opposite

Question 24

Is the minimal drive to breathe present when asleep?

Answer 24

No - in sleep, ventilation will drop down to the zero but then the arterial PCO2 will rise rapidly to exceed the apnoeic threshold and cause breathing.

Question 25

What can depress the ventilatory response to PCO2? Give a central and a peripheral example.

Answer 25

Central - disease affecting the metabolic centre or DRUGS (e.g. opioids and anaesthetics)
Peripheral - respiratory muscle weakness

Question 26

Describe the ventilatory response to a hypoxic challenge.

Answer 26

You get a 30 L/min change in minute ventilation for every 7 kPa change in PO2
So the system is MUCH LESS SENSITIVE TO PO2

Question 27

How does a high PCO2 affect the ventilatory respone to hypoxia?

Answer 27

Increased PCO2 increases the sensitivity of the response to hypoxia.
But usually it is the PCO2 that has a greater effect on control of ventilation.

Question 28

Why is this system bad at dealing with altitude where you experience hypoxic hyperventilation?

Answer 28

Hypoxic hyperventilation —> fall in PCO2 —> inhibits the ventilatory response (effect of PCO2 in increasing ventilation)

Question 29

How is neural drive different in people with COPD?

Answer 29

VT/TI seems to indicate that their neural drive is normal but, in fact, they have a MUCH HIGHER NEURAL DRIVE (if you measure diaphragm activity).
They have to try much harder to maintain the same VT/TI as normal healthy people.
This is partly because of the airway narrowing and because the hyperinflated lungs are pressing down on the diaphragm meaning that the diaphragm fibres are shorter and don’t contract as efficiently.

Question 30

How do people with obstructive disease maintain a normal minute ventilation despite breathing more shallowly?

Answer 30

Increase frequency - breathe faster

Question 31

How is the PCO2 in someone with bronchitis different to someone with emphysema?

Answer 31

Bronchitis would cause V/Q mismatch because they are breathing SHALLOWER so their PCO2 will be HIGHER
Emphysema - reduced efficiency of gas exchange - PCO2 is LOWER than bronchitis

Question 32

What are the rapid and slow responses to respiratory acidosis?

Answer 32

RAPID - ventilation changes when pH changes (alters the removal of CO2 by the lungs)
SLOW - renal compensation (kidneys can excrete weak acids e.g. lactate and keto acids)

Question 33

How is metabolic acidosis different to respiratory acidosis?

Answer 33

Source of excess H+ comes from metabolism rather than from inadequate ventilation (not due to high PCO2)

Question 34

What are the mechanisms for dealing with metabolic acidosis?

Answer 34

Increase in ventilation
Renal excretion of weak acids
Renal retention of Cl- to reduce the strong ion difference

Question 35

Give some central and peripheral causes of hypoventilation.

Answer 35

Metabolic centre poisoning - anaesthetics, drugs, chronic mountain sickness
Peripheral - muscle relaxant drugs, myasthenia gravis

Question 36

What are the three types of breathlessness?

Answer 36

Air Hunger
Increased Work and Effort
Tightness

Question 37

What scale is used to measure breathlessness?

Answer 37

Modified Borg Scale